Social Anxiety Disorder (SAD) is among the most common forms of pediatric psychopathology. These symptoms are associated with significant impairment encompassing familial, social and academic domains, and they are often comorbid with other internalizing symptoms (e.g., depression) especially in adolescence and into adulthood. Efforts to address the burden of SAD suffer from the limited understanding of its underlying pathophysiology. SAD symptoms peak in adolescence making this developmental transition an important period to study. However, considerable heterogeneity in symptomatology, risk factors, and underlying biology exists across anxious adolescents, which has implications for (1) understanding the developmental etiology of who is at highest risk, (2) identifying individual profiles of symptom course, (3) matching treatments to symptom patterns and (4) determining for whom these treatments are most effective. A substantial clinical literature exists focused on anxiety problems in children and adolescents examining clinical features with little focus on developmental processes and biological mechanisms. In contrast, the developmental literature is dominated by a temperament approach whereby extreme fearful temperament is our strongest individual differences predictor of anxiety. Exclusive focus on either model creates a barrier to progress in the field. Specifically, (1) identification of anxiety problems is typically diagnostic, with classification based solely on reported anxious behavior (rather than convergent information from different types of measures to predict a dimensional outcome); (2) we have a limited understanding of the underlying processes linking fearful temperament and anxiety across development; (3) most anxiety in children is benign, yet we lack methods to separate the true cases from false positives; and (4) although early temperament variation is ideal for identifying risk and potential mechanisms, we know little about how variation in temperament influences symptom course and effectiveness of treatments. The current study will employ a longitudinal design including continuation of a sub- sample followed since 24-months and characterized for fearful temperament. We add to this addition youth recruited for a range of SAD symptoms. Together this sampling will capture a wide range of anxiety symptom presentation (i.e., low risk, temperamental risk, and clinical anxiety). We will follow adolescents (N = 240) annually across the transitions to middle- and high-school ? ages 13, 14, 15, & 16 years. We will implement a rich assessment of anxiety symptoms, temperament, attention bias, endocrine (cortisol), physiological (RSA) and neurobiological (N1, P2, N2 evoked potentials of attention) processes. This multi-method approach aligns with the NIMH objective 2.2 to identify biomarkers and behavioral indicators of illness trajectories and explicitly tests components of the Research Domain Criteria (RDoC). Specifically, we will examine the development of the Negative Valence System of Potential Threat (?anxiety?), and the Cognitive System of Attention across multiple units of analysis including behavioral, physiological, and neural circuits.